scholarly journals Estradiol-Dependent Stimulation and Suppression of Gonadotropin-Releasing Hormone Neuron Firing Activity by Corticotropin-Releasing Hormone in Female Mice

Endocrinology ◽  
2017 ◽  
Vol 159 (1) ◽  
pp. 414-425 ◽  
Author(s):  
Chayarndorn Phumsatitpong ◽  
Suzanne M Moenter
Keyword(s):  
Gonadotropin Releasing Hormone ◽  
Corticotropin Releasing Hormone ◽  
Firing Activity ◽  
Neuron Firing ◽  
Releasing Hormone ◽  
Female Mice

Circulating maternal corticotropin-releasing hormone and gonadotropin-releasing hormone in normal and abnormal pregnancies

1996 ◽  
Vol 175 (4) ◽  
pp. 912-916 ◽  
Author(s):  
Kimberlee A. Sorem ◽  
Collin B. Smikle ◽  
Deborah K. Spencer ◽  
Brad A. Yoder ◽  
Marcia A. Graveson ◽  
...  
Keyword(s):  
Gonadotropin Releasing Hormone ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone

scholarly journals Differential Gene Expression in Gonadotropin-Releasing Hormone Neurons of Male and Metestrous Female Mice

2015 ◽  
Vol 102 (1-2) ◽  
pp. 44-59 ◽  
Author(s):  
Csaba Vastagh ◽  
Annie Rodolosse ◽  
Norbert Solymosi ◽  
Imre Farkas ◽  
Herbert Auer ◽  
...  
Keyword(s):  
Gene Expression ◽  
Differential Gene Expression ◽  
Gonadotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Female Mice ◽  
Differential Gene

scholarly journals Peripheral interleukin-1β inhibits arcuate kiss1 cells and LH pulses in female mice

2020 ◽  
Vol 246 (2) ◽  
pp. 149-160
Author(s):  
Katherine N Makowski ◽  
Michael J Kreisman ◽  
Richard B McCosh ◽  
Ali A Raad ◽  
Kellie M Breen
Keyword(s):  
Luteinizing Hormone ◽  
Cell Activation ◽  
Hormone Secretion ◽  
Receptor Activation ◽  
Gonadotropin Releasing Hormone ◽  
Interleukin 1Β ◽  
Luteinizing Hormone Secretion ◽  
Releasing Hormone ◽  
Female Mice ◽  
Neuroendocrine Function

Peripheral immune/inflammatory challenges rapidly disrupt reproductive neuroendocrine function. This inhibition is considered to be centrally mediated via suppression of gonadotropin-releasing hormone secretion, yet the neural pathway(s) for this effect remains unclear. We tested the hypothesis that interleukin-1β inhibits pulsatile luteinizing hormone secretion in female mice via inhibition of arcuate kisspeptin cell activation, a population of neurons considered to be the gonadotropin-releasing hormone pulse generator. In the first experiment, we determined that the inhibitory effect of peripheral interleukin-1β on luteinizing hormone secretion was enhanced by estradiol. We next utilized serial sampling and showed that interleukin-1β reduced the frequency of luteinizing hormone pulses in ovariectomized female mice treated with estradiol. The interleukin-1β-induced suppression of pulse frequency was associated with reduced kisspeptin cell activation, as determined by c-Fos coexpression, but not as a result of impaired responsiveness to kisspeptin challenge. Together, these data suggest an inhibitory action of interleukin-1β upstream of kisspeptin receptor activation. We next tested the hypothesis that estradiol enhances the activation of brainstem nuclei responding to interleukin-1β. We determined that the expression of interleukin-1 receptor was elevated within the brainstem following estradiol. Interleukin-1β induced c-Fos in the area postrema, ventrolateral medulla, and nucleus of the solitary tract; however, the response was not increased by estradiol. Collectively, these data support a neural mechanism whereby peripheral immune/inflammatory stress impairs reproductive neuroendocrine function via inhibition of kisspeptin cell activation and reduced pulsatile luteinizing hormone secretion. Furthermore, these findings implicate the influence of estradiol on peripherally mediated neural pathways such as those activated by peripheral cytokines.

scholarly journals MeCP2 haplodeficiency and early-life stress interaction on anxiety-like behavior in adolescent female mice

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
María Abellán-Álvaro ◽  
Oliver Stork ◽  
Carmen Agustín-Pavón ◽  
Mónica Santos
Keyword(s):  
Life Stress ◽  
Early Life ◽  
Maternal Separation ◽  
Early Life Stress ◽  
Hypothalamic Nucleus ◽  
Corticotropin Releasing Hormone ◽  
Wild Type ◽  
Releasing Hormone ◽  
Complex Disorders ◽  
Female Mice

Abstract Background Early-life stress can leave persistent epigenetic marks that may modulate vulnerability to psychiatric conditions later in life, including anxiety, depression and stress-related disorders. These are complex disorders with both environmental and genetic influences contributing to their etiology. Methyl-CpG Binding Protein 2 (MeCP2) has been attributed a key role in the control of neuronal activity-dependent gene expression and is a master regulator of experience-dependent epigenetic programming. Moreover, mutations in the MECP2 gene are the primary cause of Rett syndrome and, to a lesser extent, of a range of other major neurodevelopmental disorders. Here, we aim to study the interaction of MeCP2 with early-life stress in variables known to be affected by this environmental manipulation, namely anxiety-like behavior and activity of the underlying neural circuits. Methods Using Mecp2 heterozygous and wild-type female mice we investigated the effects of the interaction of Mecp2 haplodeficiency with maternal separation later in life, by assessing anxiety-related behaviors and measuring concomitant c-FOS expression in stress- and anxiety-related brain regions of adolescent females. Moreover, arginine vasopressin and corticotropin-releasing hormone neurons of the paraventricular hypothalamic nucleus were analyzed for neuronal activation. Results In wild-type mice, maternal separation caused a reduction in anxiety-like behavior and in the activation of the hypothalamic paraventricular nucleus, specifically in corticotropin-releasing hormone-positive cells, after the elevated plus maze. This effect of maternal separation was not observed in Mecp2 heterozygous females that per se show decreased anxiety-like behavior and concomitant decreased paraventricular nuclei activation. Conclusions Our data supports that MeCP2 is an essential component of HPA axis reprogramming and underlies the differential response to anxiogenic situations later in life.

Stress CRasHes into fertility command center

2017 ◽  
Vol 9 (415) ◽  
pp. eaaq1232
Author(s):  
Vasiliki Michopoulos
Keyword(s):  
Gonadotropin Releasing Hormone ◽  
Dependent Manner ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Command Center

Corticotropin-releasing hormone alters activity of gonadotropin-releasing hormone neurons in an estradiol-dependent manner.

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